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A 28-year-old man with a history of seasonal allergies presented to the ED for one day of diffuse body aches. He said the pain had started in his wrists and progressed to his elbows, shoulders, lower back, and knees. The pain was exacerbated by movement, and was associated with a mild, diffuse rash that lasted a couple of hours before resolving.

He had tried ibuprofen with minimal relief, and reported no fevers, upper respiratory symptoms, sick contacts, recent sexual partners, or trauma. He said, however, that the symptoms had started about an hour after surfacing from a scuba dive the day before, and his pain had progressively worsened over the next 18 hours. He had dived three times to a maximum depth of 120 feet in a single day. He did not have a dive computer, but he matched another diver's safety stops during the ascent.

His vital signs were within normal limits, and his neurologic exam was nonfocal. He had no joint deformity, redness, warmth, or swelling, and he had full passive range of motion in all joints. His cardiopulmonary exam was normal, and his ECG, chest radiograph, and labs were unremarkable except for a mild creatine kinase elevation at 1,000 U/L.

Diagnosis: Type 1 Decompression Sickness

Decompression sickness, self-reported in 1.55 of 1,000 underwater dives, results from the accumulation of gas bubbles, primarily nitrogen, in blood and tissues as the partial pressure of gas decreases during a rapid ascent from underwater diving. (Diving Hyperb Med 2014;44[2]:79.)

Besides mechanical obstruction of blood flow, the accumulation of nitrogen bubbles causes a cascade of inflammatory cytokines and thrombosis, resulting in end-organ damage and its related symptoms. (Rosen's Emergency Medicine, 8th Edition. Philadelphia: Elsevier; 2018;1773.) Nitrogen is soluble in lipid-rich tissues, so the central nervous system is particularly vulnerable. Onset of symptoms is typically within the first six hours after surfacing, although delayed symptoms can be seen up to 24 hours after the latest dive.

Several factors are known to increase the risk of decompression sickness, including longer duration and depth of dive, patient factors such as old age, obesity, dehydration, and patent foramen ovale, and environmental factors such as cold temperature, high-altitude dives, and air travel shortly after diving. (Lancet 2011;377[9760]:153.) Divers can reduce the risk of decompression sickness by using dive computers or tables that consider the depth, duration, and frequency of dives to plan decompression stops along the ascent. The use of low-nitrogen mixed gases rather than compressed air can also reduce decompression sickness at greater depths. (Rosen's Emergency Medicine: 1773.)

If decompression sickness is suspected, a thorough history should include the onset and progression of symptoms, number, duration, and depth of dives, and which gas types, dive tables, and dive computers were used. The physical exam largely focuses on hemodynamic assessment, a thorough neurologic examination, and cardiopulmonary, musculoskeletal, and skin examinations.

Decompression sickness can be divided into type 1, type 2, and arterial gas embolism. Type 1, which involves only the skin and musculoskeletal system, most commonly affects the elbows and shoulders, and sometimes produces mottling of the skin known as cutis marmorata, which is caused by venous stasis. Type 2, which involves other organ systems, often causes lower-extremity weakness and paresthesia due to a predilection for the lumbar spinal cord, but it can also affect the ears, lungs, and vestibular system. Arterial gas embolism occurs when gas is pushed across the alveolar barrier into the arterial circulation or crosses a patent foramen ovale, with the potential to cause an abrupt occlusion of the circulation to the brain, heart, or other organs. (Resuscitation 2003;59[2]:171.) A sudden loss of consciousness, focal deficits, seizures, dysrhythmia, myocardial infarction, or vertigo within 10 minutes of ascent should raise concern for embolism. (Goldman-Cecil Medicine, 24th Edition. Philadelphia: Elsevier Saunders; 2012; 574.)

Initial ED management includes 100% normobaric oxygen and intravenous fluids if dehydration is suspected; avoid volume overload because it can worsen cerebral and pulmonary edema, complicating type 2 decompression sickness. Tenoxicam, an NSAID, has been shown to reduce the number of recompressions needed, but did not modify long-term morbidity. (Cochrane Database Syst Rev 2012;[5]:CD005277.) Benzodiazepines can be used for seizures, but steroids and aspirin are not recommended.

Definitive treatment is hyperbaric oxygen therapy regardless of the type of decompression sickness. Hyperbaric therapy improves tissue oxygenation, facilitates washout of nitrogen within tissue, and reduces mechanical obstruction from bubbles. Prompt discussion with a hyperbaric specialist is essential because delays can worsen long-term morbidity. Avoid air transport to prevent further decompression at altitude if transfer is necessary to reach a hyperbaric facility. (Rosen's Emergency Medicine: 1773.)

Patients should be observed for 24 hours after hyperbaric therapy for symptom recurrence and told to avoid air travel for 72 hours. Patients with type 1 decompression sickness should avoid diving for seven days, patients with type 2 decompression sickness for four weeks. Referral for an echocardiographic bubble study should be considered in patients with a possible patent foramen ovale.

Our patient received a normal saline bolus, pain control, and 100% oxygen via nonrebreather mask without significant improvement. He was transferred via ground ambulance to a nearby facility for hyperbaric oxygen therapy, and his symptoms resolved after a single recompression treatment.

Dr. Hellmanis a senior emergency medicine resident at LAC+USC. Follow her on Twitter @hellmanjl. Dr. Burkholderis an assistant professor of clinical emergency medicine at the Keck School of Medicine at the University of Southern California. Follow him on Twitter @tayburkholder.